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R C Reeves

Publications and source records attributed to R C Reeves.

30 records · Page 2Linked to original sources
PubMed1983

Prospective randomized trial of intravenous and intracoronary streptokinase in acute myocardial infarction.

To evaluate the relative thrombolytic efficacy and complications of intracoronary vs high-dose, short-term intravenous streptokinase infusion in patients with acute myocardial infarction, we performed baseline coronary arteriography and then randomly allocated 51 patients with acute myocardial infarction to receive either intracoronary (n = 25) or intravenous (n = 26) streptokinase. Patients getting the drug by the intracoronary route received 240,000 IU of streptokinase into the infarct-related artery over 1 hr, whereas those getting the drug by the intravenous route received either 500,000 IU of streptokinase over 15 min (n = 10) or 1 million IU of streptokinase over 45 min (n = 16). Angiographically observed thrombolysis occurred in 76% (19/25) of the patients receiving intracoronary streptokinase, in 10% (1/10) of the patients receiving 500,000 IU of streptokinase intravenously, and in 44% (7/16) of the patients receiving 1 million IU of streptokinase intravenously. Among patients in whom thrombolysis was observed, mean elapsed time from onset of streptokinase infusion until lysis was 31 +/- 18 min in patients receiving intracoronary streptokinase and 38 +/- 20 min in those receiving intravenous streptokinase (p = NS). Among patients in whom intravenous streptokinase "failed," intracoronary streptokinase in combination with intracoronary guidewire manipulation recanalized only 7% (1/15). Fibrinogen levels within 6 hr after streptokinase were significantly lower in the patients receiving intravenous streptokinase (39 +/- 17 mg/dl) than the levels in those receiving intracoronary streptokinase (88 +/- 70 mg/dl) (p less than .05) but were similar 24 hr after streptokinase in the two groups. Bleeding requiring transfusion occurred in one patient in each group. Thus, in this prospective randomized trial of intracoronary vs intravenous streptokinase, hemorrhagic complications were few, although both regimens produced a systemic lytic state. Although the thrombolytic efficacy of intracoronary streptokinase was superior to that of high-dose, short-term intravenous streptokinase, the higher-dose intravenous regimen (1 million IU over 45 min) achieved thrombolysis in a significant minority (44%) of patients and might be useful therapy for patients not having access to emergency catheterization.

Adult↗
PubMed1982

Mechanism of additive effects of digoxin and quinidine on contractility in isolated cardiac muscle.

To evaluate the mechanism of the effect of the interaction of digoxin and quinidine on myocardial contractility, ferret right ventricular papillary muscles were isolated and the effects of digoxin, 4 x 10(-7) M, quinidine, 1 x 10(5) M and atropine, 1.5 x 10(-6) M, on peak developed force, peak rate of development of force (dF/dt) and time to peak tension were determined. The addition of quinidine to muscles treated with digoxin increased developed force 18 percent (p = 0.006) and dF/dt 35 percent (p = 0.001) without significantly changing time to peak tension. This effect was abolished by pretreatment with atropine. Quinidine alone increased developed force 35 percent (p less than 0.001) and dF/dt 70 percent (p less than 0.001) and decreased time to peak tension 22 percent (p less than 0.001) from pretreatment control values. Atropine alone increased developed force 17 percent (p = 0.02) and dF/dt 32 percent (p = 0.001) and decreased time to peak tension 13 percent (p = 0.003) from pretreatment control values. The addition of quinidine to muscles treated with atropine or of atropine to muscles treated with quinidine did not significantly change developed force, dF/dt or time to peak tension from values with either drug alone. It is concluded that digoxin and quinidine in these doses have additive effects of myocardial contractility, and that this interaction is at least partially mediated through antagonism of cholinergic influences by quinidine.

Animals↗
PubMed1982

Mechanism of abnormal interventricular septal motion during delayed left ventricular activation.

To evaluate the mechanism of the abnormal motion of the interventricular septum (IVS) seen echocardiographically in some patients with relatively delayed ventricular activation, we simultaneously recorded high-fidelity left and right ventricular pressures and electrograms and echocardiograms of the IVS in nine open-chest dogs. During sinus rhythm and during left IVS pacing, the IVS was activated from left to right, preejection left ventricular pressure exceeded right ventricular pressure, and IVS motion was normal. During right ventricular pacing from the outflow tract, apex, free wall or right IVS was activated from right to left, right ventricular pressure increased before left ventricular pressure and simultaneously there was an abrupt posterior IVS motion. Simultaneous pacing from the right IVS and left ventricular free wall activated the IVS from right to left and produced a normal transseptal preejection pressure gradient and normal IVS motion. Simultaneous pacing from the left IVS and right ventricular free wall activated the IVS from left to right, and produced abrupt preejection posterior IVS motion coincident with an altered transseptal pressure gradient. During right ventricular pacing, IVS motion after the abrupt preejection posterior movement was variable. Anterior motion was associated with a greater asynchrony of right and left ventricular contraction than was normal posterior motion. We conclude that abrupt preejection posterior IVS motion seen with delayed left ventricular activation from right ventricular pacing is due to passive IVS displacement from an altered transseptal pressure gradient, and subsequent IVS motion depends on the degree of asynchrony between right and left ventricular contraction.

Animals↗
PubMed1980

Effect of damaged ends in papillary muscle preparations.

The mechanical characteristics of the central segment of isolated cat papillary muscle were determined with recently developed equipment. Two small sharpened stainless steel pins, inserted transversely through the muscle, were used to mark the ends of a segment not damaged by attachments. Installation of the pins did not affect the performance of the muscle. The distance between the pins was measured and controlled to produce isometric and afterloaded isotonic contractions of the segment of the muscle between the pins. Data from such contractions were compared with traditional whole muscle measurements made on the same preparation. The isometric length-tension curve of the central segment was significantly higher than that of the whole muscle, and there was no plateau of developed force at long lengths in five of six muscles studied. In the resting state, the segment was more compliant than the whole muscle for physiologic lengths and much stiffer for longer lengths. Segment velocity and shortening were significantly higher than whole muscle velocity and shortening at comparable loads.

Animals↗
PubMed1976

Factors influencing left ventricular shortening in isolated canine heart.

To assess in the intact ventricle the steady-state influence of several mechanical variables on the extent of left ventricular midwall circumferential shortening, a pressure servo system was utilized in isolated canine hearts. The system permits continuous monitoring of ventricular volume and control of diastolic and systolic pressures. After determination of the diastolic volume at zero filling pressure (V0), a series of variably preloaded or afterloaded contractions were generated including the isovolumic state. Contractile state was manipulated in a positive (calcium, 12-18 mg/100 ml; norepinephrine, 0.4-1.4 mug/min) or negative (propranolol, 0.12-0.50 mg/min) direction. Force and length terms derived for a thick-walled sphere were expressed per cross-sectional area of muscle and length, respectively, calculated at V0. For any preload, an inverse linear (r greater than 0.96) force-shortening relation was obtained, and each line was identified by its slope and isovolumic load (sigma0). Both slope and sigma0 increased with positive inotropic agents (vis-a-vis propranolol) or increments in preload. Thus, in the intact ventricle an inverse linear relation characterizes the force-shortening relation with the amount of shortening determined by initial fiber length, afterload, and the contractile state of the myocardium.

Animals↗
PubMedDate not supplied

Potential approaches to evaluating the cardiovascular system using NMR.

The current status and some of the future possibilities for nuclear magnetic resonance imaging of the cardiovascular system have been described. With many of these possibilities there is overlap with existing techniques. For example, functional analysis of the left ventricle can be obtained using either echocardiography or radionuclide techniques. With current instrumentation and current costs, these conventional techniques could frequently provide a more cost-effective approach for morphologic and functional assessment of the cardiovascular system. Nevertheless, because of the excellent resolution, the inherent contrast, the sensitivity to blood motion, the three-dimensional nature, and the lack of ionizing radiation, the cardiovascular morphologic imaging capabilities of NMR may provide justification for such applications. However, for NMR to achieve its most important status as a cardiovascular imaging technique, some of its unique possibilities will need to be developed. These include the ability to reproducibly depict the proximal coronary arteries, to define regional myocardial blood flow distribution, to evaluate regional high energy phosphate or other metabolic activity; and to characterize myocardial disease using proton T1 and T2 alterations.

Animals↗